Objective To explore the effects of isogenous micro-grafting(MG)technology and the combined use of botulinum toxin type A(BTX-A)on hair regeneration in mice.Methods Forty-five C57BL/6 mice were randomly divided into five groups:normal saline group(NS group),MG group(MB-0 group),MG+low-dose BTX-A group(MB-2 group),MG+medium dose BTX-A group(MB-10 group),MG+high-dose BTX-A group(MB-50 group).The growth of hair on the backs of the mice was observed after the administration of the drugs,and the hair follicles were evaluated by hematoxylin-eosin(HE)staining on the 7th,14th,and 21st days of the experiment,and the expression of vascular endothelial growth factor(VEGF)and β-catenin was evaluated by immunohisto-chemical staining on day 21.Results After treatment with micrograft and botulinum toxin type A,the skin darke-ning time was shortened(P＜0.05),and the coverage rate of new hair increased on the 14 th day(P＜0.05).Compared with the NS group,the number of hair follicles increased(P＜0.05)and the expression of VEGF andβ-catenin increased in each other group.Conclusion Isogenous micro-grafting technology combined with botuli-num toxin type A has a promotional effect on hair regeneration in mice,and the mechanism may be related to the promotion of vascular growth and activation of β-catenin signaling.

Objective To investigate the effects and mechanisms of oridonin(ORI)on human keloid-derived fi-broblasts(HKF).Methods The effects of ORI on the proliferation activity of HKF were assessed using the CCK-8 assay.The experiment was divided into control and experimental groups.Cell scratch and Transwell assays were conducted to evaluate the migration and invasion capabilities of HKF.Real-time quantitative PCR(RT-qPCR)and Western blot were used to examine the impact of ORI on the expression of extracellular matrix-related mRNA and fi-bronectin 1(FN1),α-smooth muscle actin(α-SMA),type Ⅰ collagen(COL Ⅰ),and COL Ⅲ in HKF.The ex-periment was also divided into control,model,and transforming growth factor(TGF)-β1+ORI groups.RT-qPCR and Western blot were utilized to determine the effects of ORI on the expression of TGF-β1-induced mRNA and nu-cleotide-binding oligomerization domain-like receptor protein 3(NLRP3),apoptosis-associated speck-like protein containing a CARD(ASC),Smad2,Smad3,phosphorylated Smad2(p-Smad2),and p-Smad3 in HKF.Results CCK-8 assay demonstrated that the cell inhibition rate of HKF progressively increased with increasing concentra-tions of ORI.Compared with the control group,the experimental group exhibited a significant reduction in the mi-gration area at 24 hours and a decrease in the number of invasive cells.Furthermore,there was a significant down-regulation in the expression levels of FN1,α-SMA,COL Ⅰ,and COL Ⅲ(P＜0.05).In comparison with the con-trol group,the model group showed a significant upregulation in the expression of NLRP3,ASC,Smad2,Smad3,p-Smad2,and p-Smad3(P＜0.05).Relative to the model group,the TGF-β1+ORI group demonstrated a signifi-cant downregulation in the expression of NLRP3,ASC,Smad2,Smad3,p-Smad2,and p-Smad3(P＜0.05).Conclusion ORI the proliferation,migration,and invasiveness of HKF,as well as the formation and deposition of the extracellular matrix,through the blockade of the TGF-β1/Smad signaling pathway and the NLRP3-mediated in-flammatory response.

Objective: To investigate the effect and mechanism of α-lipoic acid(ALA) on the formation of hypertrophic scar(HTS) in rabbit ears. Methods: Eighteen New Zealand white rabbits were randomly divided into normal group, model group and 4%ALA group. After 28 days of treatment, the changes of scar related indexes were evaluated by hematoxylin-eosin(HE) staining, Masson pine(Masson) staining and immunohistochemical staining, the changes of oxidative stress related indexes were evaluated, and the expression of antioxidant pathway related proteins was detected by Western blotting. Results: The color, texture and volume of scar in 4%ALA group were lighter and softer than those in model group. The results of HE, Masson staining and immunohistochemical staining showed that the number of fibrous cells and the degree of fibrosis in the 4%ALA group were less than those in the model group. In the 4%ALA group, the content of malondialdehyde(MDA) was lower than that of the model group(P<0.001), the content of hydroxyproline(Hyp) was lower than that of the model group(P<0.01), the level of glutathione(GSH) was higher than that of the model group(P<0.01), the activity of T-SOD was higher than that of the model group(P<0.001). Western blotting showed that the content of NRF2 and the expression level of downstream antioxidant proteins in the 4%ALA group were higher than those in the model group. Conclusion ALA up-regulates NRF2 signal pathway to reduce the level of oxidative stress in HTS and inhibit scar proliferation in rabbit ears.